Abstract
Recent investigations in our laboratory have shown that in several individuals with familial dysalbuminemic hyperthyroxinemia (FDH) and with normal serum free thyroxine (FT4) concentration, sex hormone-binding globulin (SHBG) levels were significantly elevated in relation to normal subjects (1). The elevation in serum SHBG was not an estrogen-mediated effect, as these subjects were either in post-menopausal state or otherwise had normal levels of serum cortisol-binding globulin (CBG). Since SHBG is sensitive to thyroid hormone (TH) action and has been observed to increase in hyperthyroidism (2), the SHBG increase in FDH subjects suggested the possibility that an enhanced rate of T4 uptake might occur in this syndrome, particularly in those tissues which have direct access to protein-bound T4 (e.g., liver). To further test the hypothesis of increased T4 tissue availability in FDH syndrome, T4 uptake from normal and FDH sera studied using red blood cells, lymphocytes, and an anionic resin sponge.
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